The present invention relates to a totally implantable muscle-powered cardiac assist device to be used as an auxiliary pump in conjunction with the natural heart. In one configuration the device comprises a pair of tubular shunts coupled to the aorta and left ventricle of the heart which communicate with an elastic chamber formed in the shape of an oblate ellipsoid. Valves located within the shunts permit blood to flow from the weak or damaged left ventricle of the heart into the aorta when the elastic chamber is compressed. An alternate configuration involves the use of the elastic chamber as an extra-aortic counterpulsation device with no valve requirement.
The mechanical energy required to compress the chamber is supplied by an innervated autogenous muscle surrounding the elastic chamber. This muscle is stimulated by an implantable pulse generator in synchrony with the ventricular depolarization of the patient's heart. In operation, the contraction of the elastic chamber under the influence of a muscle tissue forces blood into the aorta. Additionally, the pulse generator provides chronic ultra-low frequency stimulation to the muscle tissue to maintain a high population of slow twitch-type muscle fibers.
The use of autogenous muscle to drive mechanical pumps is known in the art from U.S. Pat. No. 4,078,267 which discloses an artificial heart propelled by respiratory muscles. Devices of this type have enjoyed only limited success because, mammalian skeletal muscle is not capable of long-term pumping due to metabolic fatigue. Recently it has been demonstrated that chronic electrical stimulation of muscle tissue produces an adaptive transformation of muscle tissue which increases the capillary densitiy in the muscle tissue as well as the mytochondrial volume and results in an increased work capacity of the transformed muscle. Histologically, such tissue is transformed to the slow twitch-type which exhibits greatly increased resistance to fatigue.
Early experimental evaluation of skeletal muscles for myocardial augmentation was reported by Kantrowitz and McKennon. See Experimental Use of the Diaphragm as an Auxiliary Myocardium, Surgical Forum 9, Page 266, 1959. By wrapping diaphragm muscle around the heart and stimulating it via the phrenic nerve, they observed no significant hemodynamic effects; however, when employed as the counterpulsation device, they noted a short-term increase in the diastolic aortic pressure. Later, in 1964 Nakamora and Glenn utilized the diaphragm to assist atrial function. The diaphragm graft in the atrium continued to contract in response to stimulation from the phrenic nerve and served to elevate the right atrial pressure chronically. See Graft of the Diaphragm as a Functioning Substitute for the Myocardium; an Experimental Study, J Surg Res 4; 435, 1964.
Other approaches which involve the use of small spring-loaded diaphragm pumps with externally positioned flap valves have been energized by canine quadricept femorous muscles. Mechanical pumps of this type have shown outputs of 600-700 milliliters per minute.
These early studies demonstrated the potential for the use of skeletal muscles to augment ventricular action of the heart. However, this initial work indicated that a critical problem existed in the deterioration of muscle performance with continued use. Attempts at improving the hemodynamic behavior of the muscle graft by lower frequency stimulation was demonstrated by Doer, et al in 1984. See Synchronously Stimulated Skeletal Muscle Graft for Myocardial Repair, J Thorac Cardiovasc Surg 87: 325, 1984. These more recent studies demonstrated that skeletal muscle, while initially capable of hemodynamic work, fatigues rapidly even under conditions less demanding than those which are tolerated indefinitely by the cardiac muscle itself.
Although skeletal muscles contain populations of fibers which share many of the characteristics of cardiac muscle tissue, the skeletal type (I) or slow twitch fibers serve primarily a postural role in that they are required to sustain prolonged periods of activity without appreciable fatigue. However, in the tissue suitable for application to cardiac assist devices, these fibers are interspersed with at least an equal number of fast or type (II) fibers. These latter fibers have the properties suited to brief periods of intense activity, their fast contractile characteristics derive from specific contractile protein isoforms and extensive sacrotubular system and their dependence on energy derived from anaerobic glycolysis. This metabolic substrate renders the muscles susceptible to fatigue under conditions of prolonged use even at low cardiac rate duty cycles such as those demonstrated by Doer. Additionally, unlike cardiac muscle cells which contract as a synctyium, skeletal muscle fibers are normally recruited to an extent determined by the intensity of activation and in a fixed sequence. In practice, the fast fibers are the first to contract and the slow fibers are the last to contract. This structural property of the skeletal muscles minimizes the functional demand placed upon the fibers which are most susceptible to fatigue. However, the application of such tissues to cardiac assist devices require that all of the muscle tissues be recruited simultaneously and be equally active with the consequence of chronic fatigue.
Over the past fifteen years, however, a plasticity of muscle fiber type has been demonstrated in response to chronic electrical stimulation. In 1969, Salmons, et al demonstrated that the contractile speed of fast muscles could be modulated to a striking extent by continuous electrical stimulation of the motor nerve at a frequency of 10 Hz.
There is now a large body of evidence to show that fast skeletal muscles can ultimately acquire all of the physiological, biochemical, and ultrastructural characteristics of slow muscle under conditions of chronic stimulation. Such adapted muscles demonstrate a corresponding increase in the use of enzymes for aerobic metabolism and a decrease in the enzymes for glycolysis.
When a change is also involved, the contractile proteins period is reflected by an increased conversion of light to heavy chain insoforms of myosin characteristic of slow muscle tissue. As these changes progress over a period of months, the muscle mass contracts progressively more slowly and is more resistant to fatigue than initially. These recent developments have suggested that appropriately adapted skeletal muscle may be harvested to restore myocardial function through surgical procedures.
In the present application, however, chronically stimulated and transformed muscle tissue is utilized to actuate a biological pump implanted within the body and connected to the aorta for assisting a weakened or diseased ventricle in the delivery of blood to body tissues. At the present time, it is contemplated that the latissimus dorsi muscle will be dissected from the patient's back through a posterial aterial incision and mobilized, preserving its vascular and nervous structure. This pedicle will be passed into the thorax through a window created by the resection of approximately a 3 cm segment of the lateral arc of the second rib, thus permitting the insertiion of the pedicle into the thorax. The posterial lateral incision is closed, and access to the pedicle is achieved through a median sternotomy. The muscle flap will then be stretched along its striated side and wrapped around the elastic pumping chamber and closed at both ends using superficial interrupted sutures. After stretching the muscle flap around the elastomeric balloon, electrodes are then expected to be implanted, either on the nerve of the latissimus dorsi or through the muscle or both. The electrode system would then be attached to a suitable cardiomystimulator.
In this context, the present invention is directed to an optimized biological pump which exploits the ability of transformed tissue to augment the ventricular action of the heart. This invention discloses two alternate embodiments to achieve the desired goal of a totally implantable, body-compatible cardiac assist system.